He Jiafa, Deng Li, Liu Heping, Chen Taiying, Chen Shengying, Xia Shangzhou, Liu Yubin
Department of Hepatobiliary Surgery, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzho, Guangdong 510080, China.
Guangzhou Beogene Biotech CO., Ltd., Guangzho, Guangdong 510000, China.
Aging (Albany NY). 2019 Jan 26;11(2):350-370. doi: 10.18632/aging.101737.
The aim of this study was to investigate and expression and their effect on autophagy in hepatocellular carcinoma (HCC). We found that expression was low in hepatoma tissues and cells. Overexpression of decreased the activity of hepatoma cells. To analyze autophagic flux, we monitored the formation of autophagic vesicles by fluorescence protein method. Autophagy-related protein LC3B-II was accumulated and P62 was decreased, which indicated that autophagy was induced by BECN1, while could suppress this trend. Immunofluorescence assay showed that and Beclin 1 were co-located in hepatoma cells. Immunoprecipitation showed that could inhibit the autophagy of hepatoma cells by combining with Beclin 1. ELISA and co-immunoprecipitation suggested that the combination between BCL2L10 and Beclin 1 reduced the bond between Beclin 1 and PI3KC3. Based on Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, the PI3K/AKT signaling pathway was significantly upregulated in HCC. In conclusions, had a low expression in HCC tissues and cells, which could release to induce autophagy of hepatoma cells by downregulating PI3K/AKT signaling pathway.
本研究旨在探讨[具体物质]在肝细胞癌（HCC）中的表达及其对自噬的影响。我们发现[具体物质]在肝癌组织和细胞中的表达较低。[具体物质]的过表达降低了肝癌细胞的活性。为了分析自噬通量，我们通过荧光蛋白法监测自噬小泡的形成。自噬相关蛋白LC3B-II积累而P62减少，这表明自噬由BECN1诱导，而[具体物质]可抑制这一趋势。免疫荧光分析表明[具体物质]和Beclin 1在肝癌细胞中共定位。免疫沉淀表明[具体物质]可通过与Beclin 1结合抑制肝癌细胞的自噬。ELISA和免疫共沉淀表明BCL2L10与Beclin 1的结合减少了Beclin 1与PI3KC3之间的结合。基于京都基因与基因组百科全书（KEGG）通路分析，PI3K/AKT信号通路在HCC中显著上调。总之，[具体物质]在HCC组织和细胞中表达较低，其可通过下调PI3K/AKT信号通路释放[具体物质]诱导肝癌细胞自噬。
